Loss of α7 nicotinic acetylcholine receptor exacerbates adrenergic-induced cardiac damage

American Journal of Physiology-Cell Physiology 2026

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Authors: Kiany Miranda, Vanessa Pereira Teixeira, Sérgio Scalzo, Lígia Reis de Moura Estevão, Anderson Kenedy Santos, Bruno de Lima Sanches, Marcos Eliezeck, Fernando Araújo Espanhol, Henrique Abramo, Lucas Miranda Kangussu, Lucíola Silvia Barcelos, Vânia F. Prado
+3 more Marco A. M. Prado, Cibele Rocha-Resende, Sílvia Guatimosim
DOI: 10.1152/ajpcell.00839.2025
Cited by: 1
References: 30

Abstract

Although α7nAChR has been implicated in cardioprotection through its anti-inflammatory properties, the mechanisms underlying these effects remain elusive. We demonstrate that α7nAChR deficiency heightens susceptibility to adrenergic-induced injury, characterized by enhanced cardiomyocyte death and monocyte infiltration. Our findings confirm the anti-inflammatory role of α7nAChR and reveal its cell-autonomous prosurvival effects on cardiomyocytes, broadening our understanding of mechanisms driving cholinergic cardioprotection. This work positions α7nAChR as a regulator of myocardial resilience and highlights its therapeutic potential.

Fields of Study & Subjects

Nicotinic Acetylcholine Receptors Study Vagus Nerve Stimulation Research Nerve injury and regeneration

Publication details

Journal / source
American Journal of Physiology-Cell Physiology
Publisher
American Physiological Society
Volume
330
Issue
3
Pages
C706–C714
Publication date
12 January 2026
Language
EN